Spinal cord electrical stimulation is an alternative therapy for patients with chronic pain syndromes including angina. Although it has been shown to produce symptomatic relief and reduce ischaemia, doubts remain about its long-term safety. We report here for the first time the results of a follow-up study over a period of 62 months, mean 45 months (range 21-62), of 23 patients who had stimulator units implanted for intractable angina unresponsive to standard therapy. Symptomatic improvement was good and persisted in the majority with a mean (SD) change of NYHA grade from 3.1 (0.8) pre-operatively to 2.0 (0.9) (P < 0.01) immediately after operation and 2.1 (1.07) at the latest follow-up. GTN consumption fell markedly. Mean (SEM) treadmill exercise time increased from 407 (45) s with the stimulator off to 499 (46) s with the stimulator on (P < 0.01). Forty-eight hour ST segment monitoring in those with bipolar leads showed a reduction of total number and duration of ischaemic episodes. There were three deaths, none of which were sudden or unexplained and this mortality rate is acceptable for such a group of patients. Two patients had a myocardial infarction, which was associated with typical pain and not masked by the treatment. Complications related to earlier lead designs were frequent. This study confirms that spinal electrical stimulation is an effective and safe form of alternative therapy for the occasional patient whose angina is unresponsive to standard therapies.

The effectiveness of epidural spinal electrical stimulation has been studied in 14 patients with severe intractable angina unresponsive to standard therapies including bypass grafting. After implantation of the neurostimulator units the patients were assessed by a symptom questionnaire, treadmill exercise testing and right atrial pacing. There was a significant improvement of symptoms and GTN consumption fell markedly. With the neurostimulator on, exercise duration increased from a mean (CI) of 414 (153) to 478 (149) s, and total ST segment depression was less both at maximum exercise (7.1 (4.5) vs 5.6 (4.2) mm) and at 90% of the maximum control heart rate (3.5 (3.7) vs 2.6 (4.3) mm), with similar rate-pressure product at maximum exercise. With right atrial pacing the maximum heart rate reached before onset of angina was increased (143 (14) to 150 (7) b.min-1) and total ST segment depression was less at all heart rates. Benefit has persisted in some patients for over 2 years without any apparent adverse sequelae. Epidural spinal electrical stimulation is, therefore, an alternative therapy for some patients with intractable angina which has not responded to standard therapies.

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Aims Limited data are available concerning the evolution of the left atrial volume index (LAVI) in pre‐heart failure (HF) patients. The aim of this study was to investigate clinical characteristics and serological biomarkers in a cohort with risk factors for HF and evidence of serial atrial dilatation. Methods and results This was a prospective substudy within the framework of the STOP‐HF cohort (NCT00921960) involving 518 patients with risk factors for HF electively undergoing serial clinical, echocardiographic, and natriuretic peptide assessment. Mean follow‐up time between assessments was 15 ± 6 months. ‘Progressors’ (n = 39) were defined as those with serial LAVI change ≥3.5 mL/m2 (and baseline LAVI between 20 and 34 mL/m2). This cut‐off was derived from a calculated reference change value above the biological, analytical, and observer variability of serial LAVI measurement. Multivariate analysis identified significant baseline clinical associates of LAVI progression as increased age, beta‐blocker usage, and left ventricular mass index (all P < 0.05). Serological biomarkers were measured in a randomly selected subcohort of 30 ‘Progressors’ matched to 30 ‘Non‐progressors’. For ‘Progressors’, relative changes in matrix metalloproteinase 9 (MMP9), tissue inhibitor of metalloproteinase 1 (TIMP1), and the TIMP1/MMP9 ratio, markers of interstitial remodelling, tracked with changes in LAVI over time (all P < 0.05). Conclusion Accelerated LAVI increase was found to occur in up to 14% of all pre‐HF patients undergoing serial echocardiograms over a relatively short follow‐up period. In a randomly selected subcohort of ‘Progressors’, changes in LAVI were closely linked with alterations in MMP9, TIMP1, and the ratio of these enzymes, a potential aid in highlighting this at‐risk group.

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IntroductionHeart failure (HF) has hit the epidemic proportion and is incurring significant cost to the health care system. Given the major morbidity, mortality and economic burden of this condition, a prevention strategy needs careful assessment to determine its role in the future health care policy. The STOP-HF project has underlined the clinical and cost effectiveness of a biomarker driven risk stratification and intervention strategy in those at risk for HF. Supportive data to establish the widespread application of this strategy would come from a comparative analysis of patients at risk for HF and those of a new community diagnosis of HF followed in a disease management programme. To assess the importance of HF prevention, we report the morbidity, mortality and economic costs of an at-risk cohort compared to established community HF.Method1566 patients attending the HF prevention unit and rapid access clinic for possible new onset HF from 2002 up to end of 2012 were selected for this analysis. Using Doppler echocardiography, patients were categorised to stage A (risk factors for HF with no structural or functional impairment of the heart), stage B (asymptomatic LV systolic dysfunction [B-LVSD], or isolated LV diastolic dysfunction [B-LVDD]), and stage C (symptomatic HF with reduce LVEF [C-REF] or preserved LVEF [C-PEF]). Follow-up time for events was until the end of 2014. Hospitalisations were collected, confirmed by HIPE records and categorised as HF event, other cardiovascular (other-CV) event, non-cardiovascular (non-CV) event and death. In the pre-specified cost analysis, direct costs associated with emergency hospitalisations were analysed using a case-mix approach from the perspective of the healthcare provider.Result1097 patients were in stage A, 173 stage B (112 B-LVDD and 61 B-LVSD), and 296 stage C (181 C-PEF and 115 C-REF). BNP increased through the stages at 19.1 pg/mL, 62.8 pg/mL, 67 pg/mL, 185 pg/mL and 384.5 pg/mL. Figure 1 showed that the HF events and death rate increased across the spectrum. The other-CV events are higher in B-LVDD group compare to the B-LVSD group. C-REF has more other-CV events compared to C-PEF, but the non-CV events are similar. In the costing sub-study of 1,025 patients for whom detailed costing data were available, emergency CV hospitalisation costs per patient per annum were €313 ± 1222, €350 ± 1095 and €899 ± 1228 for stages A to C respectively. The data also show that emergency non-CV hospitalisation costs per patient per annum were €422 ± 1078, €560 ± 1316 and €2739 ± 4769 for stages A to C respectively, underlining a dramatic 4-fold increase emergency hospitalisation costs between stage B and C.Abstract 56 Figure 1Burden of heart failure in the communityConclusionThe clinical and costs impact of HF care escalate significantly with the development of the symptomatic phase of HF syndrome. These data along with the positive clinical and cost effectiveness analysis of the STOP-HF data underline the need for national activation of the STOP-HF strategy.

IntroductionDiabetes mellitus is an established cause of left ventricular dysfunction and a strong independent predictor of new onset heart failure. The STOP-HF Midlands project is a screening programme utilising NT-proBNP and collaborative care to detect left ventricular dysfunction in an asymptomatic diabetic cohort.Method612 diabetic patients attending the STOP-HF Midlands were included in this analysis. The demographic characteristics and biomarkers of traditional risk factor control in diabetics were recorded, including NT-proBNP. Doppler-echocardiography was performed if the NT-proBNP was >250 pg/mL. Left ventricular systolic dysfunction (LVSD) was defined as left ventricular ejection fraction of <50%. Left ventricular diastolic dysfunction (LVDD) was defined by left atrial volume index (LAVI) >34 ml/m2 with lateral E´ <10 cm/s.Result152 (mean age 71.8 years; 57.9% male) of the diabetic cohort required echocardiography, with a median NT-proBNP of 419 pg/mL [252: 808]. Treated hypertension was present in 50% of the group with use of renin angiotensin aldosterone (RAAS) modifying therapies in 60.9%. The blood pressure in this cohort was 128 mmHg ±18 (SD) over 71 mmHg±11 (SD). The total cholesterol, HDL, LDL and triglyceride were 3.8 mmol/L ±0.9 (SD), 1.4 mmol/L ±1.3 (SD), 2.2 mmmol/L ±1.0 (SD), 1.6 mmol/L ±1.2 (SD) respectively. The creatinine was 95.2 μmol/L ±28.1 (SD) and HbA1c was 48.7 mmol/mol ±13.6 (SD). 5.3% of the cohort was found to have LVSD. 28.3% patients had LVDD. 31.3% had LVSD with or without LVDD of LAVI >34 ml/m2 with lateral E <10 cm/s.ConclusionThese data demonstrate a high prevalence of significant asymptomatic left ventricular dysfunction in a community diabetic cohort despite excellent control of risk factors. Wider use of RAAS modifying therapy in this cohort might reduce the burden of this problem and slow the development to heart failure. The observations indicate that this population should be a focus of efforts to prevent heart failure.

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